New financing supports Rewind’s GPR17 remyelination programme
Rewind Therapeutics has announced additional financing to advance the development of its lead GPR17 antagonist programme, a potential disease modifying oral therapy intended to promote remyelination and restore neurological function in multiple sclerosis (MS).
MS is characterised by damage to myelin, but there are no approved therapies specifically designed to restore lost myelin and repair damaged nerves.
Rewind has revealed plans to complete key IND-enabling studies while building on a growing body of preclinical and translational evidence supporting GPR17 as a potential therapeutic target for remyelination.
Jim Van heusden, Executive Chair of Rewind Therapeutics, said: “Having secured additional funding, we are well positioned to advance our GPR17 programme towards its next value-inflection point. The recent data support both the biology and therapeutic potential of GPR17 antagonism and strengthen our confidence as we advance the program towards clinical development.”
In July 2026, Rewind scientists and collaborators at the Netherlands Institute for Neuroscience and Amsterdam UMC, published data which showed that once-daily oral treatment with a selective GPR17 antagonist accelerated remyelination and improved functional outcomes in acute and chronic models of demyelination.
A broader role for GPR17
Irene Knuesel, Chief Scientific Officer of Rewind Therapeutics, commented: “While many approaches can demonstrate new myelin formation, the critical question is whether this translates into functional recovery. Our data show that oral GPR17 antagonism improves both nerve conduction along the visual pathway and cognitive performance, supported by human MS tissue findings that reinforce the underlying biology. As we advance our lead programme through IND-enabling studies, emerging preclinical evidence also points to a broader role for GPR17 in metabolic regulation, including obesity.”
Post-mortem analysis of tissue from people with multiple sclerosis showed that GPR17-expressing oligodendrocyte precursor cells accumulate within and around demyelinated lesions, whereas remyelinated lesions exhibited little or no GPR17. These findings support the role of GPR17 as a key negative regulator of myelin repair.
In acute and chronic cuprizone models, once-daily oral treatment with a selective Rewind GPR17 antagonist accelerated remyelination of the corpus callosum and optic nerve. Importantly, treatment also resulted in functional recovery, including normalisation of visual evoked potential (VEP) latency delays and improved spatial memory performance.